Chapter 26: The Urinary System Part 2 Flashcards

1
Q

3 processes are involved in urine formation and adjustment of blood composition:

A
  1. Glomerular Filtration
  2. Tubular Reabsorption
  3. Tubular Secretion
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2
Q

Glomerular Filtration

A

is a passive and nonselective process (no metabolic energy required)
• Hydrostatic pressure forces fluids and solutes through filtration membrane into glomerular capsule
• No reabsorption into capillaries of glomerulus occur

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3
Q

Tubular Reabsorption

A

selectively returns 99% of substances from filtrate to blood in renal tubules and collecting ducts

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4
Q

Tubular Secretion

A
  • reabsorption in reverse
  • primarily occurs in the distal convoluted tubule when active transport moves substances like creatine and penicillin, from the blood into this tubule.
  • disposes of unwanted solutes, eliminates solutes that were reabsorbed, rids the body of excess K+, and controls blood pH.
  • Tubular secretion is most active in the proximal convoluted tubule, but occurs in the collecting ducts and distal convoluted tubules, as well.
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5
Q

Glomerular Blood Hydrostatic Pressure (GBHP) or Hydrostatic Pressure in Glomerular Capillaries (HPgc)

A
  • It is the pressure of blood in the glomerular capillaries
  • Chief force pushing water & solutes out of blood
  • Glomerular Blood Pressure: 55 mmHg
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6
Q

Capsular Hydrostatic Pressure (CHP) or Hydrostatic pressure in capsular space (HPcs)

A
  • Opposing force to GBHP by fluid already in the capsular space that tends to push water and solutes out of the filtrate and back into plasma
  • results from the resistance to flow along the nephron and conducting system
  • Filtrate Pressure in Capsule: 15 mm Hg
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7
Q

Blood Colloid Osmotic Pressure (BCOP) or Colloid osmotic pressure in capillaries (OPgc)

A
  • pressure exerted by the proteins in the plasma which tends to retain fluid and also oppose filtration
  • pulls fluid into capillaries from interstitial spaces
  • “Pull” of Proteins in Blood: 30 mm Hg
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8
Q

Explain what is meant from NFP

A

Net Filtration Pressure (NFP): sum of forces
• Pressure responsible for filtrate formation
• Main controllable factor determining Glomerular Filtration Rate (GFR)

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9
Q

How is Net Filtration Pressure calculated?

A

NFP = GBHP (outward pressures) - (CHP + BCOP) (inward pressures)
= 55 - (15 + 30) -> NFP = 10 mm Hg

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10
Q

What forces determine filtration pressure?

A
  1. Glomerular (blood) hydrostatic pressure GHP or GBHP
  2. Capsular Hydrostatic Pressure (CHP)
  3. (Blood) Colloid Osmotic Pressure (BCOP)
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11
Q

Glomerular Filtration Rate (GFR) is influenced by

A
  1. Net filtration pressure
  2. Total surface area for filtration
  3. filtration membrane permeability
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12
Q

What is the relationship between glomerular filtration rate (GFR) and NFP?

A
  • Primary factor that influences GFR (primary pressure is glomerular blood hydrostatic pressure (GBHP)
  • Increase NFP = Increase GFR (directly proportional)
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13
Q

How does total surface area for filtration influence the rate of glomerular filtration rate?

A

Glomerular mesangial cells control by contracting

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14
Q

How does filtration membrane permeability influence glomerular filtration rate?

A

Much more permeable than other capillaries

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15
Q

How is GFR regulated?

A
  1. intrinsic controls (renal autoregulation)

2. extrinsic controls

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16
Q

Why is it important to maintain a constant GFR?

A

Constant GFR is important as it allows kidneys to make filtrate and maintain extracellular homeostasis

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17
Q

Increased GFR causes

A

increased urine output, which lowers blood pressure, and vice versa

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18
Q

Intrinsic Controls: Renal Autoregulation of GFR

A

-Main goal is to maintain GFR in the kidney
-Maintains nearly constant GFR when MAP is in range of 80–180 mm Hg
• Autoregulation stops if out of that range

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19
Q

2 Types of Renal Autoregulation:

A
  1. Myogenic Mechanism

2. Tubuloglomerular Feedback Mechanism

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20
Q

Myogenic Mechanism

A

Local smooth muscle (walls of afferent arteriole) contracts when stretched
– Increased MAP or Decreased MAP
Both help maintain normal GFR despite normal fluctuations in systemic blood pressure (MAP)

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21
Q

What happens when MAP is increased during the myogenic mechanism?

A

constriction of afferent arterioles:

  • Reduces blood flow into glomerulus -> decreases GBHP
  • Protects glomeruli from damaging high BP
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22
Q

What happens when MAP is decreased during the myogenic mechanism?

A

dilation of afferent arterioles:

-Increases blood flow into glomerulus -> increases GBHP

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23
Q

Tubuloglomerular Feedback Mechanism

A

Flow-dependent mechanism directed by macula densa cells of JGA

 - Respond to:
       - filtrate’s NaCl concentration (filtrate’s osmolarity) &/or 
        - flow of filtrate in renal tubules
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24
Q

Extrinsic Controls

A

– Purpose of extrinsic controls is to regulate GFR to maintain systemic blood pressure
– Extrinsic controls will override renal intrinsic controls if blood volume needs to be increase

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25
Q

What mechanisms do extrinsic controls use?

A
  1. Neural Mechanisms

2. Hormonal Mechanisms

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26
Q

Neural Mechanisms

A

Sympathetic Nervous System
• During Rest:
– Renal blood vessels (including afferent & efferent arterioles): dilate
– Renal autoregulation mechanisms prevail
• During Stress or Emergency: Low BP/blood volume (blood loss; excessive fluid loss – chronic diarrhea, frequent vomiting; dehydration) or High BP (exercise)
– Norepinephrine is released by sympathetic nervous system and epinephrine is released by adrenal
medulla

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27
Q

Release of norepinephrine and epinephrine by neural mechanisms causes

A
  • Systemic vasoconstriction (including renal blood vessels): increases blood pressure, and reduces blood flow to the kidneys
  • Strong constriction of afferent arterioles: significantly decreases GFR (decrease in urine output)
    • Blood Volume and Blood Pressure: Increase
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28
Q

Hormonal Mechanisms

A
  1. Atrial Natriuretic Peptide (ANP)

2. Renin-Angiotensin-Aldosterone System (RAAS)

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29
Q

Atrial Natriuretic Peptide (ANP)

A
  • released by cells of the atria when blood pressure/blood volume increases
  • causes relaxation of glomerular mesangial cells -> increases capillary surface area -> increases GFR
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30
Q

Renin-Angiotensin-Aldosterone System (RAAS)

A
  • when blood pressure/blood volume decreases -> main mechanism for increasing blood pressure/blood volum
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31
Q

3 Pathways to Renin release by Juxtaglomerular Cells (Granular Cells):

A
  1. Direct stimulation of granular cells by sympathetic nervous system
  2. Stimulation by activated macula densa cells when filtrate NaCl concentration is low
  3. Reduced stretch of granular cells
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32
Q

Anuria

A

abnormally low urinary output (less than 50 ml/day)
• May indicate that glomerular blood pressure is too low to cause filtration
• Renal failure and anuria can also result from situations in which nephrons stop functioning
– Example: acute nephritis, transfusion reactions, and crush injuries

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33
Q

What are the two routes of tubular reabsorption?

A
  1. transcellular route

2. paracellular route

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34
Q

Transcellular Route (Transcellular Reabsorption)

A
  • Solute enters apical membrane of tubule cells
  • Travels through cytosol of tubule cells
  • Exits basolateral membrane of tubule cells
  • Enters blood through endothelium of peritubular capillaries
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35
Q

Paracellular Route (Paracellular Reabsorption)

A

Between tubule cells
– Limited by tight junctions, but leaky in PCT
» Water, Ca2+, Mg2+, K+, and some Na+ in the PCT move via this route

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36
Q

Proximal Convoluted Tubule (PCT)

A

– Site of most reabsorption:
• All nutrients, such as glucose and amino acids, are 100% reabsorbed
• 65% of Na+, K+ and water reabsorbed
• Many ions (passive diffusion): 50% Cl-, 80% - 90% bicarbonate, variable amounts of calcium and phosphate • 50% of urea

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37
Q

Tubular Reabsorption of Sodium

A
  1. transported across apical membrane

2. transported across basolateral membrane

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38
Q

What happens to sodium as it is transported across the apical membrane?

A

Na+ enters tubule cell at apical surface via secondary active transport (cotransport) or via facilitated diffusion through channels:
- Active pumping of Na+ at basolateral membrane results in strong electrochemical gradient within tubule cell
– Results in low intracellular Na+ levels that facilitates Na+ diffusion

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39
Q

Sodium transported across basolateral membrane

A

– Na+ is most abundant cation in filtrate
– Transport of Na+ across basolateral membrane of tubule cell is via primary active transport
– Na+-K+ ATPase pumps Na+ into interstitial space
– Na+ is then swept by bulk flow into peritubular capillaries

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40
Q

Transport Maximum

A

Transcellular transport systems are specific and limited
– Transport maximum (Tm) exists for almost every reabsorbed substance and reflects number of carriers in renal tubules that are available
-When carriers for a solute are saturated, excess is excreted in urine

41
Q

Reabsorption Rates of Nephron Loop

A
Reabsorbs:
water: 15%
bicarbonate ion: 10-20% 
Na+ & K+: 20-30% 
Ca2+ & Mg2+: variable amount 
Cl-: 35%
42
Q

Reabsorption in the descending limb of the nephron loop

A

in the descending limb, H2O can leave, solutes cannot

43
Q

Reabsorption in the ascending limb of the nephron loop

A

H2O cannot leave, solutes can :
• Thin segment is passive to Na+ movement
• Thick segment has Na+-K+-2Cl– symporters and Na+-H+ antiporters that transport Na+ into cell
– Some Na+ can pass into cell by paracellular route in this area of limb

44
Q

Distal Convoluted Tubule (DCT) and Collecting Duct Reabsorption

A
  • Initial Part of DCT: reabsorption of:
    • Water: 10-15%
    • Na+: 5%
    • Cl-:5%
    • Major site of PTH (parathyroid hormone) stimulates reabsorption of Ca2+
45
Q

In the last part of DCT & Collecting Duct, reabsorption is regulated by

A

hormones (ADH, aldosterone, Atrial Natriuretic Peptide (ANP), Parathyroid Hormone (PTH))

46
Q

Antidiuretic hormone (ADH)

A

increase water reabsorption
• Released by posterior pituitary gland
• Causes principal cells of collecting ducts and latter part of DCT to insert aquaporins in apical membranes ->
increasing water reabsorption

47
Q

Aldosterone

A
  • increase blood pressure and decrease K+ levels
  • Targets principal cells of collecting ducts
  • Promotes synthesis of: apical Na+-Cl-symporter and K+ channels, and basolateral Na+-K+ ATPases for Na+ reabsorption (H2O follows, if it can)
  • As a result, little Na+ leaves body
48
Q

Without aldosterone

A

daily loss of filtered Na+ would be 2%, which is incompatible with life.

49
Q

Where is aldosterone produced in the body?

A

produced in the cortex of the adrenal glands

50
Q

Atrial Natriuretic Peptide (ANP)

A

– Reduces Na+ and water reabsorption at PCT and Collecting Ducts –> resulting in decreased blood volume & BP
– Released by cardiac atrial cells if blood volume or blood pressure elevates

51
Q

Parathyroid Hormone (PTH)

A

Acts on initial part of DCT to increase Ca2+ reabsorption and inhibits phosphate reabsorption in the PC

52
Q

ADH Inhibitors

A

alcohol

53
Q

Na+ Reabsorption Inhibitors

A

Caffeine

54
Q

What is the chemical composition of human urine?

A

made up of 95% water and 5% solutes:
-nitrogenous wastes: 1. urea (from amino acid breakdown): largest solute component, 2. uric acid (from nucleic acid metabolism), 3. creatine (metabolite of creatine phosphate)
-Other normal solutes found in urine: Na+, K+, PO4
3–, and SO42–, Ca2+, Mg2+ and HCO3

55
Q

What are the physical characteristics of urine?

A
  1. Color and Transparency
  2. Odor
  3. pH
  4. Specific Gravity
56
Q

Physical Characteristic of Urine: Color and Transparency

A

• Clear: Cloudy may indicate urinary tract infection
• Pale to deep yellow from urobilin
-Pigment from hemoglobin breakdown: Yellow color deepens with increased concentration
• Abnormal color (pink, brown, smoky): Can be caused by certain foods, bile pigments, blood, drug

57
Q

Physical Characteristic of Urine: Odor

A
  • Slightly aromatic when fresh
  • Develops ammonia odor upon standing as bacteria metabolize urea
  • May be altered by some drugs or vegetables
  • Disease may alter smell: ex) Patients with diabetes may have acetone smell to urine
58
Q

Physical Characteristic of Urine: pH

A
  • Urine is slightly acidic (~pH 6, with range of 4.5 to 8.0)
  • Acidic diet (protein, whole wheat) can cause drop in pH • Alkaline diet (vegetarian), prolonged vomiting, or urinary tract infections can cause an increase in pH
59
Q

Physical Characteristic of Urine: Specific Gravity

A
  • Ratio of mass of substance to mass of equal volume of water (specific gravity of water = 1)
  • Ranges from 1.001 to 1.035 because urine is made up of water and solute
60
Q

Diuretics

A

Chemicals that enhance urinary output by decreasing water reabsorption:

  • ADH inhibitors
  • Na+ Reabsorption Inhibitors
  • Loop Diuretics
  • Osmotic Diuretics
61
Q

Loop Diuretics

A

inhibit Na+-K+-2Cl- symporters (thick ascending limb of nephron loop) - inhibit medullary gradient
formation

62
Q

Osmotic Diuretics

A

substance not reabsorbed, so water remains in urine

63
Q

Chronic renal disease

A

defined as a GFR

64
Q

Renal failure

A

defined as GFR

65
Q

hemodialysis

A
  • a machine filters wastes, salts and fluid from your blood when your kidneys are no longer healthy enough to do this work adequately
  • is the most common way to treat advanced kidney failure.
66
Q

incontinence

A

the loss of bladder control

67
Q

hypernatremia

A
  • excess of the electrolyte Sodium (Na+)
  • may occur with dehydration, water deprivation or excessive sodium in diet or intravenous fluids
  • causes hypertonicity of ECF which pulls water out of body cells into ECF, causing cellular dehydration
68
Q

Signs and Symptoms of hypernatremia

A

intense thirst, hypertension, edema, agitation and convulsions

69
Q

hyponatremia

A
  • deficiency of the electrolyte Sodium (Na+)
  • may be due to:
    • decreased sodium intake
    • increased sodium loss through vomiting, diarrhea or taking certain diuretics
    • excessive water intake
70
Q

hypokalemia

A
  • excess of electrolyte potassium (K+)
  • may be due to excessive pottasium intake, renal failur, aldosterone deficiency, crushing injuries to body tissues or transfusion of hemolyzed blood.
71
Q

hypokalemia

A
  • deficiency of electrolyte potassium (K+)
  • may result from excessive loss due to vomiting diarrhea, decreased potassium intake, hyperaldosteronism, kidney disease, and therapy with some diuretics
72
Q

hypocalcemia

A
  • deficiency of electrolyte calcium (Ca2+)

- may be due to increased calcium loss, reduced calcium intake, elevated phosphate levels or hypoparathyroidism

73
Q

hypercalcemia

A
  • excess of electrolyte calcium (Ca2+)

- may result from hyperparathyroidism, some cancers, excessive intake of vitamin D, and Paget’s disease of bone

74
Q

Physiology of the Kidney

A

~ 180 L (47 gallons) of blood-derived fluid processed daily, but only 1 - 2 L of urine is formed
• Kidneys filter body’s entire plasma volume 60 times each day
• Consume 20–25% of oxygen used by body at rest
• Filtrate (produced by glomerular filtration): blood plasma minus large to medium-sized proteins & blood cells

75
Q

Urine

A

• Urine is produced from filtrate

76
Q

Outward Pressures

A

forces that promote filtrate formation

includes glomerular blood hydrostatic pressure (GBHP) or Hydrostatic pressure in glomerular capillaries (HPgc)

77
Q

Inward Pressures

A
  • forces inhibiting filtrate formation

- includes capuslar hydrostatic pressure (CHP) and blood colloid osmotic pressure (BCOP)

78
Q

Where does tubular secretion occur?

A

occurs almost completely in PCT, but also in cortical parts of collecting ducts and late regions of the DCT

79
Q

Tubular secretion is important for:

A
  1. Disposing of substances, such as drugs or metabolites, that are bound to plasma proteins
  2. Eliminating undesirable substances that were passively reabsorbed (example: urea and uric acid)
  3. Ridding body of excess K+ (aldosterone effect)
  4. Controlling blood pH by altering amounts of H+ or HCO3
    – in urine
80
Q

Filtration Membrane

A

Porous membrane between blood and interior of glomerular capsule
– Allows water and solutes smaller than plasma proteins to pass (Normally no cells can pass)

81
Q

What are the three layers of the filtration membrane?

A
  1. Fenestrated Endothelium of glomerular capillaries (Pore)
  2. Basal Lamina of Glomerulus
  3. Slit Membrane: Foot Processes of Podocytes (Pedicel) with filtration slits
82
Q

Function of the fenstrated endothelium of glomerular capillaries

A

prevents filtration of blood cells but allows all components of blood plasma to pass through

83
Q

Function of the basal lamina of glomerulus

A

prevents filtration of larger proteins

84
Q

Function of slit membrane between pedicels

A

prevents filtration of medium-sized proteins

85
Q

What provides energy and means for reabsorbing almost every other substances (nutrients, water, ions)?

A

Na+ reabsorption by primary active transport

86
Q

Secondary Active Transport

A

– Electrochemical gradient created by pumps at basolateral surface give “push” needed for transport of other solutes
– Organic nutrients reabsorbed by secondary active transport are cotransported with Na+ via Na+-symporters
• Glucose, amino acids, some ions, vitamin

87
Q

Passive Tubular Reabsorption of Water

A

– Movement of Na+ and other solutes creates osmotic gradient for water
– Water is reabsorbed by osmosis, aided by water-filled pores called aquaporins: obligatory and facultative water reabsorption

88
Q

Obligatory water reabsorption

A

– Aquaporins are always present in PCT and Descending Limb of Nephron Loops

89
Q

Facultative water reabsorption

A

– Aquaporins are inserted in collecting ducts only if ADH is present

90
Q

Passive Tubular Reabsorption of Solutes

A
  • Solute concentration in filtrate increases as water is reabsorbed (Creates concentration gradients for solutes, which drive their entry into tubule cell and peritubular capillaries)
    – Fat-soluble substances, some ions, and urea will follow water into peritubular capillaries down their concentration gradients
91
Q

Urea helps form medullary gradient:

A
  1. Urea enters filtrate in ascending thin limb of nephron loop by facilitated diffusion
  2. Cortical collecting duct reabsorbs water, leaving urea behind
  3. In deep medullary region, now highly concentrated urea leaves collecting duct and enters interstitial fluid of medulla
    • Urea then moves back into ascending thin limb
    • Contributes to high osmolality in medulla
92
Q

glycosuria

A

glucose in urine

possible causes is diabetes mellitus

93
Q

proteinuria or albuminuria

A

proteins in urine

causes: non pathological:excessive physical exertion, pregnancy
pathaological: glomerulonephritis, severe hypertension, heart failure, often sign of renal disease

94
Q

ketonuria

A

ketone bodies in urine

causes: excessive formation and accumulation of ketone bodies, as in starvation and untreated diabetes melitus

95
Q

hemoglobinuria

A

hemoglobin in urine

causes: various: transfusion reaction, hemolytic anemia, severe burns

96
Q

bilirubinuria

A

bile pigments in urine

causes: liver disease or obstruction of bile ducts from liver or gallbladder

97
Q

hematuria

A

erythrocytes in urine

causes: bleeding urinary tract

98
Q

pyuria

A

leukocytes in urine

causes: urinary tract infection